Natriuretic peptides and peripheral autonomic neurotransmission: back to the A, B, and C's.

Abstract

This editorial refers to ‘C-type natriuretic peptide and natriuretic peptide receptor NPR-B signalling inhibits cardiac sympathetic neurotransmission and autonomic function’ by J. Buttgereit et al. , pp. 637–644. Natriuretic peptides (NPs) are a family of secretory peptides that have in common a ringed amino-acid structure linked by disulphide bonds1 which signal via NP receptors (NPRs). Three primary members have been identified: atrial NP (ANP), brain-derived NP (BNP), and C-type NP (CNP), but there is a closely related forth peptide Dendroaspis NP (DNP). ANP and BNP are elevated by atrial stretch; ventricular stretch or stress elevates BNP levels; and all NPs are increased in heart failure (HF). The NPRs are particulate guanylyl-cyclase-coupled receptors which stimulate production of cGMP. Of the seven NPR isoforms known to exist, the majority of NP physiological actions are mediated via NPR-A and -B, while NPR-C mediates NP degradation. ANP, BNP, and DNP activate NP receptor A (NPR-A), which increases natriuresis and vasodilation. In contrast, CNP specifically activates NPR-B and does not possess the potent diuretic actions of the other NPs. Although extensive studies have been performed on BNP in the context of HF, where it has been utilized both as a diagnostic and as a potential therapeutic tool,2 newer data implicate the peptide in modulating peripheral autonomic neurotransmission. BNP activation of NPR-A inhibits neurotransmission from sympathetic neurons by decreasing …